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Kourdova, L. T.

Publications and source records attributed to Kourdova, L. T..

2 recordsLinked to original sources

An oomycete effector that induces shade avoidance like growth and suppresses plant defenses targets the AUX/IAA protein IAA11

Filamentous pathogens, such as oomycetes, employ multiple strategies to suppress plant immunity, one of which involves manipulating phytohormone signaling pathways. The effector HaRxL106 from Hyaloperonospora arabidopsidis (Hpa), known to induce shade avoidance syndrome (SAS)-like growth, has previously been shown to interact with brassinosteroid signaling components. Here, we investigate the role of HaRxL106 in altering auxin signaling, revealing that HaRxL106 targets the AUX/IAA protein IAA11, a key negative regulator of auxin responses. Our data suggest that HaRxL106 impedes the repressive function of IAA11, enhancing auxin signaling and promoting SAS, which concurrently suppresses plant immune responses. These findings provide insights into how pathogen effectors manipulate plant growth and immunity to facilitate infection.

plant biology↗

Downy mildew effector HaRxL106 interacts with the transcription factor BIM1 altering plant growth, BR signaling and susceptibility to pathogens

Hyaloperonospora arabidopsidis (Hpa) is an oomycete pathogen that causes downy mildew disease on Arabidopsis. This obligate biotroph manipulates the homeostasis of its host plant by secreting numerous effector proteins, among which are the RxLR-effectors. Identifying the host targets of effectors and understanding how their manipulation facilitates colonization of plants is key to improve plant resistance to pathogens. Here we characterize the interaction between the RxLR effector HaRxL106 and BIM1, an Arabidopsis transcription factor (TF) involved in Brassinosteroid (BR) signaling. We report that HaRxL106 interacts with BIM1 in vitro and in planta. BIM1 is required by the effector to increase the host plant susceptibility to (hemi)biotrophic pathogens, and thus can be regarded as a susceptibility factor. Mechanistically, HaRxL106 requires BIM1 to induce the transcriptional activation of BR-responsive genes and cause alterations in plant growth patterns that phenocopy the shade avoidance syndrome. Our results support previous observations of antagonistic interactions between activation of BR signaling and suppression of plant immune responses and reveal that BIM1, a new player in this crosstalk, is manipulated by the pathogenic effector HaRxL106. SIGNIFICANCE STATEMENTOur study reveals that the Arabidopsis transcription factor BIM1 plays a key role as a susceptibility factor that is manipulated by the oomycete effector HaRxL106 to induce the Brassinosteroid (BR) signaling pathway and suppress plant immunity. HaRxL106 induces BIM1-dependent expression of BR-responsive genes which affects normal plant growth generating a shade avoidance-like syndrome that impacts negatively on plant defenses against bacterial and oomycete pathogens.

plant biology↗